Plus d’anticorps contre PDGFRB partenaires d’interaction

PDGFR signaling is necessary for postnatal tendon growth and remodeling and MT1-MMP is a critical mediator of tendon fibroblast migration.

PDGFR alpha beta and PDGFR beta beta dimers were strong inducers of random and directionally-persistent migration in mouse skin fibroblast, respectively, that was sustained for up to 24 h.

PDGFRbeta was activated around the injury site after experimental traumatic brain injury (TBI), and primarily expressed in astrocytes, microglia, OPC and leukocytes in the boundary of the lesion site, suggesting PDGFRbeta was involved in glial scar formation. Then the PDGFR inhibitor (AG1296) was administered following TBI. Reactive astrocytes were significantly inhibited in AG1296-treated mice.

The data of this study revealed an acute accumulation of PDGFRbeta+ BBB-related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRbeta-signaling in blood vessel and post-injury tissue recovery.

Beta platelet-derived growth factor is induced in hepatic stellate cells (HSCs) following surgical partial hepatectomy, and its deletion in HSCs leads to prolonged liver injury in mice. However, there is no significant difference in liver regeneration.

The results provide functional evidence that elevated PDGFRbeta signaling causes tissue wasting or overgrowth reminiscent of human genetic syndromes and that the STAT1 pathway is a crucial modulator of this phenotypic spectrum.

Identify PDGFRbeta as a driver in activating Akt/mTORC1 nexus for high glucose-mediated expression of collagen I (alpha2) in proximal tubular epithelial cells, which contributes to tubulointerstitial fibrosis in diabetic nephropathy.

Data show that three platelet-derived growth factor receptor beta (PDGFRB) mutants (R561C, P660T and N666K) were able to transform NIH3T3 and Ba/F3 cells to different extents.

data therefore collectively suggest that upon TGFbeta stimulation, SP1 recruits SMAD2 to the promoter of Pdgfrb to up-regulate its expression and thus Pdgfrb is a direct downstream target of the TGFbeta/SMAD2 signaling

PdgfrbetaF7/F7 mice between 4-6 and 36-48 weeks of age developed a region-dependent loss in pericyte coverage (22-46, 24-44 and 4-31%) and cell numbers (36-49, 34-64 and 11-36%), reduction in capillary length (20-39, 13-46 and 1-30%), and an increase in extravascular fibrinogen-derived deposits (3.4-5.2, 2.8-4.1 and 0-3.6-fold) demonstrating BBB breakdown in the cortex, hippocampus and thalamus, respectively.

PDGF-B-PDGFRbeta signaling plays a significant role in the development of adipose tissue neovascularization.

there is great possibility that EPCs overexpressing PDGFR-beta enhanc VSMC apoptosis and suppress VSMC migration by competitive consumption of PDGF-BB in the early phase after carotid artery injury in mice.

PDGFRalpha and PDGFRbeta are coexpressed in the craniofacial mesenchyme of mid-gestation mouse embryos and that ablation of Pdgfrb in the neural crest lineage results in increased nasal septum width, delayed palatal shelf development, and subepidermal blebbing.

The results from this study indicate that PDGF signaling is required for fiber hypertrophy, extracellular matrix production, and angiogenesis that occur during muscle growth.

Decreased expression of PDGFR-beta in vascular smooth muscle cells was associated with thrombosis in vivo.

Our results highlight the need for careful interpretation of lineage tracing using constitutive Cre lines that cannot discriminate active from historical expression. The early vascular targeting by the Pdgfrb-Cre also warrants consideration for its use in studies of mural cells

Study demonstrated that LRIG2 promoted the PDGFRBinduced proliferation of glioblastoma multiforme cells in vitro and in vivo through regulating the PDGFRB signalingmediated cell cycle progression.

High expression of PDGFR-beta in prostate cancer stroma is independently associated with clinical and biochemical prostate cancer recurrence.

Study investigated the more detailed mechanism for this cis-interaction of Necl-5 with the PDGF receptor beta. Necl-5 contains three Ig-like domains and the PDGF receptor beta contains five Ig-like domains at their extracellular regions; showed that the third Ig-like domain of Necl-5 cis-interacted with the fifth Ig-like domain of the PDGF receptor beta.

Study revealed that high PDGFRbeta expression in cancer tissue was an independent marker of poor prognosis relating to recurrence in patients with colorectal cancer.

High GLI2 or PDGFRB expression is associated with unfavorable survival in GC patients. GLI2 can induce PDGFRB expression in GC cells via directly binding to its promoter. In addition, the GLI2-PDGFRB axis might be an important signaling pathway modulating CSC properties of GC cells.

The cell surface PDGFRB is a major link between high glucose and its effectors Hif1a and TGFB for induction of diabetic mesangial cell hypertrophy.

describes three unique PDGFRB fusions in childhood B- or T-ALL. All three PDGFRB fusion partners have previously been reported to be implicated in hematopoiesis and immune responses

These findings indicated that miR-518b may function as a tumor suppressor by targeting PDGFRB in the occurrence and development of GBM.

Data show that an equilibrium mixture of two unusual end-insertion G-quadruplexes forms in a native promoter sequence and appears to be the molecular recognition for platelet derived growth factor receptor beta (PDGFR-beta) downregulation.

These findings indicate that the levels of phosphorylated PDGFR-beta are decreased in endothelial progenitor cells with the in vitro expansion process, which impairs their angiogenic potential by inhibiting PI3K/Akt signaling.

PDGFRB profil antigène

Antigen Summary

This gene encodes a cell surface tyrosine kinase receptor for members of the platelet-derived growth factor family. These growth factors are mitogens for cells of mesenchymal origin. The identity of the growth factor bound to a receptor monomer determines whether the functional receptor is a homodimer or a heterodimer, composed of both platelet-derived growth factor receptor alpha and beta polypeptides. This gene is flanked on chromosome 5 by the genes for granulocyte-macrophage colony-stimulating factor and macrophage-colony stimulating factor receptor\; all three genes may be implicated in the 5-q syndrome. A translocation between chromosomes 5 and 12, that fuses this gene to that of the translocation, ETV6, leukemia gene, results in chronic myeloproliferative disorder with eosinophilia.